Chest Pain Epidemiology

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1 Chest Pain Epidemiology6 million ED visits/year5-7% ED patients3.3% AIS evacuations 2002, 3.5% in 2003, % in 2004, 3.2% in 20053 million patients admitted/year70% found not to have acute coronary event0.4% - 4.0% acute MI are sent home

2 Chest Pain PathophysiologyChest pain syndromes difficult to diagnoseMultiple organ systems of the chestShare afferent (nerve) pathwaysPathology in any of these systems have similar pattern of complaintsMost patients have CP with acute coronary syndrome(ACS), others may present with only SOB, N/V, arm or jaw pain

3 Differential Diagnosis of Chest PainLife-threatening causesAcute coronary syndrome(ACS)Aortic dissectionPulmonary embolismTension pneumothoraxEsophageal rupture (Boerhaave’s syndrome)Pericarditis; myocarditisAcute chest syndrome(in sickle cell disease)Myocarditis is the most common cause of sudden death in the young. Acute chest syndrome is the most common cause of death in sickle cell patients. Sickle cell patients presenting with chest pain should be presumed to have acute chest syndrome until proven otherwise. Progressive hypoxia, multilobar pneumonia, on chest x-ray, and falling hemoglobin levels are the most common clinical findings.

8 History“The most important difference between a good and indifferent clinician lies in the amount of attention paid to the story of the patient”---Farquhar Buzzard

9 HistoryHelpful to group questions to target the three most common life threats;Consider ACS questionsPulmonary embolism(PE) questionsAortic dissection questions

10 History Cardiac Questions2 most important historical informationage, genderAdvancing age, prevalence and severity of CAD increasesCan estimate pretest probability of CAD based on age and genderFurther refine pretest probability by classifying the chest pain as typical, atypical, or non-anginalCAD(coronary artery disease). A combination of autopsy data and large angiography studies allows us to estimate the pretest probability of CAD in patients based on age and gender alone.

12 Pretest likelihood of CAD based on age, sex, and symptomsAtypical angina Typical anginaAge Men Women Men Women% % % %% % % %% % % %% % % %Atypical(variant) angina or Prinzmetal angina primarily occurs at rest and without provocation. The current thought is that variant angina is due to vasospasm of the coronary vessels. When studies are performed by angiogram, about 1/3 have no or insignificant atherosclerosis and about 2/3 have CAD in addition to spasm.

14 Cardiac Questions Character of PainMany patients have atypical symptomsAsk questions in regard to nature (quality), severity(1-10), duration, modifying factors of the pain, and associated symptoms40% patients with AMI have atypical CP35% patients without AMI have typical CP

15 Cardiac QuestionsIn one study of 721 patients who were diagnosed with AMI, almost ½ presented without CPSOB, weakness, dizziness, syncope, abdominal painTypical angina is a deep, poorly localized chest or arm discomfort that is classically exertional and relieved with rest or nitrates

20 Aortic Dissection HistoryMale (75%)Seventh decadeHistory of hypertension (70%)Other risk factors;Marfan’s syndrome, atherosclerosis, prior dissection, or known aortic aneurysmMarfan”s syndrome is a generalized disorder of connective tissue with skeletal, ocular, and cardiac manifestations. The extremities are long and thin. The eyes show subluxation of the lens. Severe myopia and spontaneous retinal detachment are common. Cardiovascular defects include disruption and loss of elastic fibers in the media of the aorta. The lack of elasticity results in progressive diffuse dilatation of the proximal segment of the ascending aorta and severe aortic regurgitation. Heart failure and rupture of the aorta from dissecting aneurysm are the most common cause of death.

21 Aortic Dissection HistoryPain is sudden onset (83%)Severe or “worse ever” (90%)Sharp (64%) or tearing (50%)Location anterior chest (60%), back (53%)Migratory (16%), radiating (28%)Suspect dissection in patients with clinical changing picturePatients who complain of chest pain along with a neurologic deficit may have a dissection occluding a cerebral or spinal artery.

22 Aortic Dissection HistoryShould address 3 basic concerns regarding a patient’s pain:quality (sudden and severe)radiation (especially to the back)intensity at onset (maximal)Aortic dissection and MI can coexist8% dissection involves coronary arteriesOne retrospective study showed that when all three questions were asked, physicians correctly diagnosed thoracic aortic dissection in 30 of 33 patients(91%); if one or more of these aspects were omitted, the correct diagnosis was suspected in fewer than half of all patients.EKG changes such as acute ST and T wave abnormalities are present in half of all patients with aortic dissection--- often confounding the initial diagnosis.

23 Pulmonary Embolism HistoryClinical diagnosis of PE is difficultSymptoms are variable and nonspecificCan range from dyspnea and fatigue to severe pleuritic CP and syncopeClassic description of pleuritic pain, dyspnea, and hemoptysis represents embolic pulmonary infarction and is seen most commonly in hospitalized patients

28 Other ConditionsBoerhaave’s syndrome presents as spontaneous esophageal rupture after vomitingPain on swallowingSignificant number are recently, or acutely intoxicatedPericarditis refers pain to neck, shoulder and worsens with inspiration, swallowing, and lying supine

29 Physical ExaminationStable patients with AMI rarely have physical findings on examVital SignsChest pain and hypotension-not good8% PE and 15% aortic dissection are hypotensive on presentationPatients with CP and hypotension are 3 times more likely to have AMI than normotensive pts

31 Physical Examination Vital Signs Tachycardia is nonspecific signMay be only clue to early pericarditis, myocarditisBradycardia, esp. due to conduction defects, may be seen in right coronary occlusions

33 Physical Examination Head and NeckCheck neck for Kussmaul’s sign (a paradoxical increase in jugular venous distension with inspiration)Seen in pericardial tamponade, right heart failure or infarction, PE, or tension pneumothorax)Subcutaneous air at the root of the neck suggests pneumothorax, or pneumomediastinitisCarotids bruits increase likelihood of CAD

35 Physical Examination Pulmonary ExamWheezing and rales are important findings but are not specific for certain diseasesAsthma, foreign body, CHF, PE all may cause wheezingRales are rare in pts with AMI, but their presence with left heart failure, raises the likelihood of MI by twofold

36 Physical Examination Cardiac ExamA new murmur may signal papillary muscle ruptureMurmur of aortic insufficiency is an important finding associated with aortic dissectionS3 gallop secondary to CHF raises likelihood of MI 3 times

38 Physical Examination Chest Wall ExamEven with chest wall tenderness, still have to consider life-threatening causesReproducible CP frequently seen in pts with PE and ACSCostochondritis is inflammation of the costal cartilages, may result in sharp, dull, or pleuritic CP, rarely has swelling of soft tissues

40 Physical Examination Exam of the ExtremitiesLook for edema, thrombosis, or pulse deficitsPeripheral edema frequently seen in right-sided and biventricular failureUsually absent in acute left heart failureUnilateral edema or palpable venous thrombus(cord) suggest DVT or PEBut most pts with PE have normal ext. exams

41 Physical Examination Examination of PulsesExam for symmetry and qualityPulse deficit is defined as asymmetrical amplitude between the right and left sidesPulse deficits most common in type A dissections(ascending aorta)Measured BP difference occurs 15%Differences > 20mmHg between arms was an independent predictor of dissection

43 Diagnostic StudiesThe ECG is the most important test in the evaluation of CPThe initial ECG is insensitive in identifying acute coronary syndromeOnly 20%-60% pts presenting with acute MI have diagnostic changes on initial ECG

44 Diagnostic Studies ECGWhat diagnostic changes?at least 1 mm elevation in one or more inferior/lateral leadsor at least 2mm of elevation in one or more anterioseptal leads10% pts with AMI have LVH with repolarization changesTall peaked T waves may be earliest sign of AMI